Equine Pleuropneumonia Study Guide

Overview and Clinical Importance

Pleuropneumonia represents a severe manifestation of bronchopneumonia defined as bacterial infection of the lungs that extends to include the visceral pleura and pleural space. This condition is frequently encountered in equine practice and represents a significant category of respiratory disease on the NAVLE. It is often referred to as shipping fever due to its strong association with long-distance transport.

Pleuropneumonia is the most severe form of pneumonia in horses and often requires long-term hospitalization and intensive care. Horses with pleuropneumonia frequently develop systemic inflammatory response syndrome (SIRS) and endotoxemia, which can lead to complications including laminitis and death. Survival rates range from 40% to 90% depending on the severity of disease, timing of intervention, and presence of anaerobic bacteria.

Etiology and Pathophysiology

Risk Factors

Pleuropneumonia is typically associated with a predisposing condition that compromises pulmonary defense mechanisms, allowing secondary bacterial infection to occur. The primary risk factor is long-distance transport, which compromises lower respiratory tract defenses through multiple mechanisms.

Pathophysiology Stages

Pleuropneumonia develops through three progressive pathophysiological stages that are important for understanding disease progression and guiding treatment decisions.

Bacterial Etiology

Pleuropneumonia typically involves polymicrobial and mixed anaerobic-aerobic infections. Bacteria are usually normal inhabitants of the oropharynx that overwhelm compromised pulmonary defenses. Different organisms may be isolated from tracheal aspirate versus pleural fluid.

Clinical Signs and Presentation

Clinical findings in horses with pleuropneumonia vary according to the stage and severity of disease. The condition does not always develop immediately and can go unnoticed for days to weeks after the inciting event.

S - Stiff gait and stance with abducted elbows H - History of transport or anesthesia I - Inappetence and depression P - Pleural pain (pleurodynia) P - Pyrexia (fever greater than 101.5°F) I - Increased respiratory rate (shallow) N - No lung sounds ventrally G - Gross nasal discharge (bilateral)

Diagnostic Approach

Thoracic Ultrasonography

Thoracic ultrasonography is the preferred diagnostic modality for pleuropneumonia. It is more sensitive than radiography for detection of pleural disease and can be performed in ambulatory settings.

Sample Collection and Analysis

Tracheobronchial Aspirate (TBA)

TBA is ESSENTIAL in horses with pleuropneumonia and often yields better culture results than pleural fluid. Can be obtained via percutaneous or endoscopic-guided aspiration. Submit for Gram stain, cytology, and aerobic/anaerobic culture with sensitivity.

Pleural Fluid Analysis (Thoracentesis)

Laboratory Findings

Treatment

The three pillars of therapy for pleuropneumonia are: (1) Antimicrobial therapy, (2) Drainage of pleural effusion, and (3) Supportive care. Early, aggressive treatment is critical for optimal outcomes.

Antimicrobial Therapy

Initial empirical therapy should provide broad-spectrum coverage against aerobic gram-positive, gram-negative, AND anaerobic organisms. IV administration is preferred for optimal tissue levels. Treatment duration is typically several weeks to months.

Pleural Drainage

Drainage decisions are based on ultrasonographic findings and pleural fluid character. Not all cases require drainage - moderate effusions may resorb with antimicrobial therapy alone.

• Thoracentesis: Preferred site is 6th-7th intercostal space, just dorsal to costochondral junction. Use ultrasound guidance for safety. Sample BOTH sides of chest.
• Indwelling Chest Tube: Indicated when continued fluid accumulation makes intermittent thoracentesis impractical. Attach Heimlich valve to prevent pneumothorax. Can remain in place for several weeks.
• Pleural Lavage: Controversial efficacy. May help remove debris and fibrin. Sterile saline infusion followed by drainage.
• Intrapleural Fibrinolytics (rTPA): Recombinant tissue plasminogen activator to dissolve fibrin. Efficacy debated. Survival rates with TPA approximately 72% vs 68% without.

Supportive Care

• NSAIDs: Flunixin meglumine (1.1 mg/kg IV q12-24h) or phenylbutazone for analgesia, anti-inflammatory effect, and anti-endotoxin properties.
• IV Fluids: Replace third-space losses. Large volumes may be lost daily through pleural drainage.
• Laminitis Prevention: CRITICAL. Distal limb cryotherapy (ice boots). Monitor digital pulses closely.
• Nutrition: High caloric intake essential - high metabolic demands. Fresh water and variety of feeds. Consider omeprazole for GI protection.
• Environment: Dust-free, well-ventilated stabling. Supplemental oxygen if needed.

Surgical Intervention

Thoracotomy is indicated when prolonged medical management fails, particularly with extensive fibrin accumulation, abscessation, or walled-off lesions. Can be performed under standing sedation or general anesthesia. Procedures include drainage, rib resection, abscess removal, and lung lobectomy. Surgery survival rate is approximately 88% with 46% return to racing potential.

Prognosis and Complications

Survival Rates

• Overall survival: 40-90% depending on severity and timing of treatment
• Aerobic infections: 30-66% survival
• Anaerobic infections: 21-50% survival (has improved with metronidazole use)
• Return to athletic performance: Approximately 60% of survivors

Negative Prognostic Indicators

• Increased serum creatinine at presentation
• Anaerobic bacterial isolates
• Free gas echoes in pleural fluid
• Necrotizing pneumonia
• Fibrinous effusion and extensive fibrin accumulation
• Pulmonary or cranial thoracic abscesses
• Bronchopleural fistula
• Klebsiella spp. or Actinobacillus spp. isolates

Complications

• Laminitis: Secondary to SIRS/endotoxemia (8% of cases in one study)
• Thrombophlebitis: Secondary to IV catheter placement
• Antimicrobial-associated diarrhea/colitis: Monitor for changes in fecal consistency
• Pneumothorax: Secondary to bronchopleural fistula or iatrogenic
• DIC: Coagulopathy from severe sepsis

Exam Focus: Remember: the prognosis has improved over the past 20 years due to early recognition, diagnostic advances, and aggressive treatment. Horses that recover have a reasonable chance of returning to athletic performance (approximately 61% return to racing).

P - Putrid odor (anaerobes) O - Organization stage with pleural peel O - Oxygen needed (gas echoes = poor) R - Renal azotemia (elevated creatinine) S - SIRS and septic shock I - Increased fibrin/loculations G - Gas-producing bacteria N - Necrosis of lung tissue S - Stubborn (Klebsiella, Actinobacillus)